ArticleJournal of virology2009
Interaction of ICP34.5 with Beclin 1 modulates herpes simplex virus type 1 pathogenesis through control of CD4+ T-cell responses.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 4 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
101 citing papers in PubMed, 4 syntheses or guidelines pooled it, 138 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Autophagy modulation in animal models of corneal diseases: a systematic review.Molecular and cellular biochemistry · 2020Pooled it
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Guideline
- Differential Sensitivity of HSV-1 and PRV to IFN-λ Reveals a Neuron-Specific Antiviral Role for RSAD2.bioRxiv : the preprint server for biology · 2026Article
- From infection to dysfunction: viral triggers and antiviral immune factors in Alzheimer's disease pathology.Frontiers in immunology · 2026Review
- Herpes Simplex Virus Neurovirulence Across the Human Lifespan.The Journal of infectious diseases · 2025Review
- TRIM23 mediates cGAS-induced autophagy in anti-HSV defense.Nature communications · 2025Article
- Asymptomatic neonatal herpes simplex virus infection in mice leads to persistent CNS infection and long-term cognitive impairment.PLoS pathogens · 2025Article
- Advanced progress in the genetic modification of the oncolytic HSV-1 virus.Frontiers in oncology · 2024Review
- SARS-CoV-2 Harnesses Host Translational Shutoff and Autophagy To Optimize Virus Yields: the Role of the Envelope (E) Protein.Microbiology spectrum · 2023Article
- PKR induces TGF-β and limits oncolytic immune therapy.Journal for immunotherapy of cancer · 2023Article
- AUTOPHAGY IN THE EYE: FROM PHYSIOLOGY TO PATHOPHYSOLOGY.Autophagy reports · 2023Article
- Autophagy as a dual-faced host response to viral infections.Frontiers in cellular and infection microbiology · 2023Review
- Autophagy in the normal and diseased cornea.Experimental eye research · 2022Review
- Blocking Autophagy in M1 Macrophages Enhances Virus Replication and Eye Disease in Ocularly Infected Transgenic Mice.Journal of virology · 2022Article
- Interplay between Autophagy and Herpes Simplex Virus Type 1: ICP34.5, One of the Main Actors.International journal of molecular sciences · 2022Review
- The molecular regulation of autophagy in antimicrobial immunity.Journal of molecular cell biology · 2022Article
- Exosomes and autophagy in ocular surface and retinal diseases: new insights into pathophysiology and treatment.Stem cell research & therapy · 2022Review
- Interactions of Autophagy and the Immune System in Health and Diseases.Autophagy reports · 2022Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Autophagy is an important component of host innate and adaptive immunity to viruses. It is critical for the degradation of intracellular pathogens and for promoting antigen presentation. Herpes simplex virus type 1 (HSV-1) infection induces an autophagy response, but this response is antagonized by the HSV-1 neurovirulence gene product, ICP34.5. This is due, in part, to its interaction with the essential autophagy protein Beclin 1 (Atg6) via the Beclin-binding domain (BBD) of ICP34.5. Using a recombinant virus lacking the BBD, we examined pathogenesis and immune responses using mouse models of infection. The BBD-deficient virus (Delta68H) replicated equivalently to its marker-rescued counterpart (Delta68HR) at early times but was cleared more rapidly than Delta68HR from all tissues at late times following corneal infection. In addition, the infection of the cornea with Delta68H induced less ocular disease than Delta68HR. These results suggested that Delta68H was attenuated due to its failure to control adaptive rather than innate immunity. In support of this idea, Delta68H stimulated a significantly stronger CD4(+) T-cell-mediated delayed-type hypersensitivity response and resulted in significantly more production of gamma interferon and interleukin-2 from HSV-specific CD4(+) T cells than Delta68HR. Taken together, these data suggest a role for the BBD of ICP34.5 in precluding autophagy-mediated class II antigen presentation, thereby enhancing the virulence and pathogenesis of HSV-1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.